Neurogenic inflammation can be triggered by activation of nociceptive and thermal-sensitive nerve endings in tissues. Such activation can be caused by tissue injury, viral infection, or innate conditions, such as autoimmune disease. For example, once an individual has been infected with the herpes virus, the virus will thereafter remain latent in the body. In the latent state, the virus can settle in nerve cell bodies in the ganglia. Stimuli, such as influenza infection, other respiratory disorders, gastrointestinal infections, stress, fatigue, menstruation, pregnancy, allergy, sunlight, or fever, can activate the latent virus, which may then travel from the ganglia to the skin surface and multiply, causing various symptoms. Exemplary symptoms include pain, neurogenic inflammation, blistering, and other somatosensory system manifestations such as, for example, pain, itch, tickle, tingle, and numbness.
At the onset of such symptoms, conventional methods for the treatment of pain and inflammation are often initiated, for example, non-steroidal anti-inflammatory drugs (NSAIDs), antidepressants, and antiviral medications (e.g., acyclovir, famciclovir, or valacyclovir). Such conventional methods often fall short of true treatment by only providing temporary relief, masking symptoms and/or causing serious side effects from prolonged use. Thus, there remains a need for a safe and effective treatment of inflammation and pain which can be used without the side effects associated with long-term use of conventional treatments.